| Literature DB >> 30395541 |
Patrick Maffucci1,2, Jose Chavez1, Thomas J Jurkiw3, Patrick J O'Brien3, Jordan K Abbott4, Paul R Reynolds4, Austen Worth5, Luigi D Notarangelo6, Kerstin Felgentreff7, Patricia Cortes8, Bertrand Boisson9,10, Lin Radigan1, Aurélie Cobat10,11, Chitra Dinakar12, Mohammad Ehlayel13, Tawfeg Ben-Omran14, Erwin W Gelfand4, Jean-Laurent Casanova9,10,11,15,16, Charlotte Cunningham-Rundles1,2.
Abstract
We report the molecular, cellular, and clinical features of 5 patients from 3 kindreds with biallelic mutations in the autosomal LIG1 gene encoding DNA ligase 1. The patients exhibited hypogammaglobulinemia, lymphopenia, increased proportions of circulating γδT cells, and erythrocyte macrocytosis. Clinical severity ranged from a mild antibody deficiency to a combined immunodeficiency requiring hematopoietic stem cell transplantation. Using engineered LIG1-deficient cell lines, we demonstrated chemical and radiation defects associated with the mutant alleles, which variably impaired the DNA repair pathway. We further showed that these LIG1 mutant alleles are amorphic or hypomorphic, and exhibited variably decreased enzymatic activities, which lead to premature release of unligated adenylated DNA. The variability of the LIG1 genotypes in the patients was consistent with that of their immunological and clinical phenotypes. These data suggest that different forms of autosomal recessive, partial DNA ligase 1 deficiency underlie an immunodeficiency of variable severity.Entities:
Keywords: B cells; Genetic diseases; Genetics; Immunology; T cell development
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Year: 2018 PMID: 30395541 PMCID: PMC6264644 DOI: 10.1172/JCI99629
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 14.808